Skip to main content
Fig. 4 | Stem Cell Research & Therapy

Fig. 4

From: Histone hypo-acetylation of Sox9 mediates nicotine-induced weak cartilage repair by suppressing BMSC chondrogenic differentiation

Fig. 4

Effects of nicotine on Sox9 and NFATc2 expression in BMSCs. Assay was performed after 24 h of in vitro culture. a mRNA expression of Sox9 in BMSCs with stimulus of nicotine for 8 h. b mRNA expression of Sox9 in BMSCs with stimulus of nicotine for 16 h. c mRNA expression of Sox9 in BMSCs with stimulus of nicotine for 24 h. d and e Protein expression of Sox9 in BMSCs with stimulus of nicotine for 24 h. f and g Expression of NFATc2 in nucleoproteins with stimulus of nicotine for 24 h. h and i Expression of phosphorylated NFATc2 in the cytoplasm with stimulus of nicotine for 24 h. j and k Expression of NFATc2 in total protein with stimulus of nicotine for 24 h. l and m Effect of Si-NFATc2 in BMSCs. n and o Effects of MLA and Si-NFATc2 on nicotine’s suppression of Sox9 in BMSCs. Data represent mean ± SEM (n = 3). *p < 0.05, **p < 0.01. BMSCs bone marrow mesenchymal stem cells, Col2A1 α1 chain of type II collagen, MLA methyllycaconitine, NFATc2 nuclear factor of activated T cell 2, Sox9 SRY-type high-mobility group box 9

Back to article page